Asthma and lower airway diseaseIncreased sputum and bronchial biopsy IL-13 expression in severe asthma
Section snippets
Subjects
Subjects were recruited from local primary health care providers, respiratory clinics, hospital staff, and through local advertising. Asthma was defined and severity categorized by using international (Global Initiative for Asthma [GINA]) guidelines15 and American Thoracic Society criteria for refractory asthma.14 Healthy subjects had no history of respiratory symptoms and normal spirometric results. All subjects provided written informed consent, with study approval from the Leicestershire
Results
Clinical and sputum characteristics for subjects in cohort 1 are shown in Table I. The groups with asthma were well matched for AHR and sputum eosinophilic inflammation. The sputum IL-13 concentration for each subject is shown in Fig 1. The proportion of subjects with measurable IL-13 in their sputum supernatant was increased in those with severe asthma (10/26) and mild asthma (15/34) compared with the proportion of healthy control subjects (4/32, P < .05). In addition, the proportion of
Discussion
For the first time, we have shown that sputum IL-13 concentration and the number of IL-13+ cells in the bronchial submucosa and ASM bundle were increased in severe asthma. We have confirmed our earlier observation that mast cell localization to the ASM bundle is a feature of mild asthma2 and demonstrated for the first time that this is also characteristic of moderate and severe refractory disease. Interestingly, in contrast to severe asthma, increased sputum IL-13 concentrations and IL-13+
References (35)
- et al.
Sputum and bronchial submucosal IL-13 expression in asthma and eosinophilic bronchitis
J Allergy Clin Immunol
(2004) - et al.
Interleukin-13 and interleukin-5 in induced sputum of eosinophilic bronchitis: comparison with asthma
Chest
(2005) - et al.
Elevated expression of messenger ribonucleic acid encoding IL-13 in the bronchial mucosa of atopic and nonatopic subjects with asthma
J Allergy Clin Immunol
(1997) - et al.
New insights into the relationship between airway inflammation and asthma
Clin Sci (Lond)
(2002) - et al.
Mast-cell infiltration of airway smooth muscle in asthma
N Engl J Med
(2002) - et al.
Eosinophilic bronchitis is an important cause of chronic cough
Am J Respir Crit Care Med
(1999) - et al.
Immuno-regulatory cytokines in asthma: IL-15 and IL-13 in induced sputum
Clin Exp Allergy
(2001) - et al.
Interleukin-4 and -13 expression is co-localized to mast cells within the airway smooth muscle in asthma
Clin Exp Allergy
(2003) - et al.
Expression of IL-12 and IL-13 mRNA in asthma and their modulation in response to steroid therapy
Am J Respir Crit Care Med
(1997) - et al.
Evaluation of airway inflammation by quantitative Th1/Th2 cytokine mRNA measurement in sputum of asthma patients
Thorax
(2006)
IL-13 expression at the sites of allergen challenge in patients with asthma
J Immunol
Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
J Clin Invest
Requirement for IL-13 independently of IL-4 in experimental asthma
Science
Proceedings of the ATS Workshop on Refractory Asthma. Current understanding, recommendations, and unanswered questions
Am J Respir Crit Care Med
Pathological features and inhaled corticosteroid response of eosinophilic and non-eosinophilic asthma
Thorax
Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999
Am J Respir Crit Care Med
Cited by (232)
The Unified Airway Hypothesis: Evidence From Specific Intervention With Anti–IL-5 Biologic Therapy
2023, Journal of Allergy and Clinical Immunology: In PracticeCurrent Limitations and Recent Advances in the Management of Asthma
2023, Disease-a-MonthWhat has been learned by cytokine targeting of asthma?
2022, Journal of Allergy and Clinical ImmunologyPathology of Asthma
2021, Encyclopedia of Respiratory Medicine, Second Edition
Supported by Asthma UK, Cambridge Antibody Technology, GlaxoSmithKline, and a DOH Clinical Scientist award.
Disclosure of potential conflict of interest: C. E. Brightling has consulting arrangements with AstraZeneca, GlaxoSmithKline, Cambridge Antibody Technology, and Roche; has received research support from AstraZeneca, Cambridge Antibody Technology, and GlaxoSmithKline; and is on the speakers' bureau for GlaxoSmithKline, AstraZeneca, and Pfizer. R. May is employed by and has equity in Cambridge Antibody Technology. P. Monk is employed by Synairgen Research Ltd. I. D. Pavord has received research support from GlaxoSmithKline and AstraZeneca. The rest of the authors have declared that they have no conflict of interest.